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MBC in Press, published online ahead of print May 30, 2007
Mol. Biol. Cell 10.1091/mbc.E06-12-1147

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Submitted on December 26, 2006
Revised on May 14, 2007
Accepted on May 23, 2007

The Clathrin Adaptor Complex AP-1 Binds HIV-1 and MLV Gag and Facilitates Their Budding

Grégory Camus,*{dagger}{ddagger} Carolina Segura-Morales,{ddagger}{sect} Dorothee Molle,{sect} Sandra Lopez-Vergès,*{dagger} Christina Begon-Pescia,{sect} Chantal Cazevieille,|| Peter Schu,¶ Edouard Bertrand,{sect} Clarisse Berlioz-Torrent,*{dagger}# and Eugenia Basyuk{sect}#

*Centre National de la Recherche Scientifique (Unité Mixte de Recherche 8104) and {dagger}Institut National de la Santé et de la Recherche Médicale U567, Institut Cochin, Université Paris Descartes, 75014 Paris, France; {sect}Institut de Génétique Moléculaire de Montpellier-Centre National de la Recherche Scientifique, Unité Mixte de Recherche 5535, 34293 Montpellier, France; ||Centre Régional d’Imagerie Cellulaire/Institut Universitaire de Recherche Clinique, 34093 Montpellier, France; University of Göttingen, Center for Biochemistry and Molecular Cell Biology, Biochemistry II, 37073 Göttingen, Germany

Monitoring Editor: Jennifer Lippincott-Schwartz

Retroviral assembly is driven by Gag, and nascent viral particles escape cells by recruting the machinery that forms intralumenal vesicles of multi-vesicular bodies. In this study, we show that the clathrin adaptor complex AP-1 is involved in retroviral release. The absence of AP-1µ obtained by genetic knock-out or by RNA-interference reduces budding of MLV and HIV-1, leading to a delay of viral propagation in cell culture. In contrast, overexpression of AP-1µ enhances release of HIV-1 Gag. We show that the AP-1 complex facilitate retroviral budding through a direct interaction between the matrix and AP-1µ. Less MLV Gag is found associated with late endosomes in cells lacking AP-1, and our results suggest that AP-1 and AP-3 could function on the same pathway that leads to Gag release. In addition, we find that AP-1 interacts with Tsg101 and Nedd4.1, two cellular proteins known to be involved in HIV-1 and MLV budding. We propose that AP-1 promotes Gag release by transporting it to intracellular sites of active budding, and/or by facilitating its interactions with other cellular partners.

{ddagger}These authors contributed equally to this work.

#These authors contributed equally to this work.

Address correspondence to: Clarisse Berlioz-Torrent (Berlioz{at}cochin.inserm.fr) or Eugenia Basyuk (Eugenia.Basyuk{at}igmm.cnrs.fr)




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